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Abstract
Lipocalin 2 (Lcn2), an innate immune protein, has emerged as a critical iron regulatory
protein during physiological and inflammatory conditions. As a bacteriostatic factor,
Lcn2 obstructs the siderophore iron-acquiring strategy of bacteria and thus inhibits
bacterial growth. As part of host nutritional immunity, Lcn2 facilitates systemic,
cellular, and mucosal hypoferremia during inflammation, in addition to stabilizing
the siderophore-bound labile iron pool. In this review, we summarize recent advances
in understanding the interaction between Lcn2 and iron, and its effects in various
inflammatory diseases. Lcn2 exerts mostly a protective role in infectious and inflammatory
bowel diseases, whereas both beneficial and detrimental functions have been documented
in neurodegenerative diseases, metabolic syndrome, renal disorders, skin disorders,
and cancer. Further animal and clinical studies are necessary to unveil the multifaceted
roles of Lcn2 in iron dysregulation during inflammation and to explore its therapeutic
potential for treating inflammatory diseases.